Tourism and economic development in a cash-in-advance economy

This paper examines the impact of tourism on welfare in a cash-in-advance economy. As a result of the expansion in tourism, the price of the non-traded good increases. This gives rise to a terms-of-trade improvement. However, the cash-in-advance constraint causes a distortion in consumption. For tourism demand, where the gain from the terms-of-trade improvement dominates (does not dominate) the loss from the consumption distortion, tourism is welfare-improving (welfare-reducing). A similar condition for welfare improvement (deterioration) holds for a model of capital inflow and endogenised tourism.

Is money targeting an option for Bank Indonesia?

In this paper, using the cash-in-advance model, we estimate Indonesia's money demand function for the period 1970–2005. We find the real M1 and real M2 are cointegrated with their determinants, namely real income, real exchange rate and short-term domestic and foreign interest rates. The long-run elasticities, except for the relationship between M2 and domestic interest rate, are plausible. Interestingly, we find a negative relationship between real exchange rate and real money demand, suggesting evidence of currency substitution. We test for causal relationships and find that in the short-run only the real exchange rate Granger causes real M1 and real M2. Finally, we find that Indonesia's money demand functions are unstable. We conclude that money targeting is not an option for Bank Indonesian and that currency substitution should be curbed in order to ensure macroeconomic sustainability.

Estimating money demand functions for South Asian countries

In this paper, we estimate a money demand function for a panel of five South Asian countries. We find that the money demand and its determinants, namely real income, real exchange rate and short-term domestic and foreign interest rates are cointegrated both for individual countries as well as for the panel, and panel long-run elasticities provide robust evidence of statistically significant relationships between money demand and its determinants. Our test for panel Granger causality suggests short-run causality running from all variables, except foreign interest rate, to money demand, and we find evidence that except for Nepal money demand functions are stable.

Copper-dependent iron assimilation pathway in the model photosynthetic eukaryote chlamydomonas reinhardtii

The unicellular green alga Chlamydomonas reinhardtii is a valuable model for studying metal metabolism in a photosynthetic background. A search of the Chlamydomonas expressed sequence tag database led to the identification of several components that form a copper-dependent iron assimilation pathway related to the high-affinity iron uptake pathway defined originally for Saccharomyces cerevisiae. They include a multicopper ferroxidase (encoded by Fox1), an iron permease (encoded by Ftr1), a copper chaperone (encoded by Atx1), and a copper-transporting ATPase. A cDNA, Fer1, encoding ferritin for iron storage also was identified. Expression analysis demonstrated that Fox1 and Ftr1 were coordinately induced by iron deficiency, as were Atx1 and Fer1, although to lesser extents. In addition, Fox1 abundance was regulated at the posttranscriptional level by copper availability. Each component exhibited sequence relationship with its yeast, mammalian, or plant counterparts to various degrees; Atx1 of C. reinhardtii is also functionally related with respect to copper chaperone and antioxidant activities. Fox1 is most highly related to the mammalian homologues hephaestin and ceruloplasmin; its occurrence and pattern of expression in Chlamydomonas indicate, for the first time, a role for copper in iron assimilation in a photosynthetic species. Nevertheless, growth of C. reinhardtii under copper- and iron-limiting conditions showed that, unlike the situation in yeast and mammals, where copper deficiency results in a secondary iron deficiency, copper-deficient Chlamydomonas cells do not exhibit symptoms of iron deficiency. We propose the existence of a copper-independent iron assimilation pathway in this organism.

Application of radial return mapping algorithm for finite strain elastoplasticity in a hybrid finite element and particle-in-cell model

The radial return mapping algorithm within the computational context of a hybrid Finite Element and Particle-In-Cell (FE/PIC) method is constructed to allow a fluid flow FE/PIC code to be applied solid mechanic problems with large displacements and large deformations. The FE/PIC method retains the robustness of an Eulerian mesh and enables tracking of material deformation by a set of Lagrangian particles or material points. In the FE/PIC approach the particle velocities are interpolated from nodal velocities and then the particle position is updated using a suitable integration scheme, such as the 4th order Runge-Kutta scheme[1]. The strain increments are obtained from gradients of the nodal velocities at the material point positions, which are then used to evaluate the stress increment and update history variables. To obtain the stress increment from the strain increment, the nonlinear constitutive equations are solved in an incremental iterative integration scheme based on a radial return mapping algorithm[2]. A plane stress extension of a rectangular shape J2 elastoplastic material with isotropic, kinematic and combined hardening is performed as an example and for validation of the enhanced FE/PIC method. It is shown that the method is suitable for analysis of problems in crystal plasticity and metal forming. The method is specifically suitable for simulation of neighbouring microstructural phases with different constitutive equations in a multiscale material modelling framework.

Conjugated linoleic acid suppresses myogenic gene expression in a model of human muscle cell inflammation

Proinflammatory cytokines, such as tumor necrosis factor (TNF)-{alpha}, contribute to muscle wasting in inflammatory disorders, where TNF{alpha} acts to regulate myogenic genes. Conjugated linoleic acid (CLA) has shown promise as an antiproliferative and antiinflammatory agent, leading to its potential as a therapeutic agent in muscle-wasting disorders. To evaluate the effect of CLA on myogenesis during inflammation, human primary muscle cells were grown in culture and exposed to varying concentrations of TNF{alpha} and the cis-9, trans-11 and trans-10, cis-12 CLA isomers. Expression of myogenic genes (Myf5, MyoD, myogenin, and myostatin) and the functional genes creatine kinase (CK) and myosin heavy chain (MHC IIx) were measured by real-time PCR. TNF{alpha} significantly downregulated MyoD and myogenin expression, whereas it increased Myf5 expression. These changes corresponded with a decrease in both CK and MHC IIx expression. Both isomers of CLA mimicked the inhibitory effect of TNF{alpha} treatment on MyoD and myogenin expression, whereas myostatin expression was diminished in the presence of both isomers of CLA either alone or in combination with TNF{alpha}. Both isomers of CLA decreased CK and MHC IIx expression. These findings demonstrate that TNF{alpha} can have specific regulatory effects on myogenic genes in primary human muscle cells. A postulated antiinflammatory role of CLA in myogenesis appears more complex, with an indication that CLA may have a negative effect on this process.

EBSD study of the orientation dependence of substructure characteristics in a model Fe-30wt%Ni alloy subjected to hot deformation

The aim of the present investigation was to determine the orientation dependence of substructure characteristics in an austenitic Fe−30wt%Ni model alloy subjected to hot plane strain compression. Deformation was carried out at a temperature of 950 °C using a strain rate of 10 s^₋₁ to equivalent strain levels of approximately 0.2, 0.4, 0.6 and 0.8. The specimens obtained were analysed using a fully automatic electron backscatter diffraction technique. The crystallographic texture was characterized for all the strain levels studied and the subgrain structure was quantified in detail at a strain of 0.4. The substructure characteristics displayed pronounced orientation dependence. The major texture components, namely the copper, S, brass, Goss and rotated Goss, generally contained one or two prominent families of parallel larger-angle extended subboundaries, the traces of which on the longitudinal viewing plane appeared systematically aligned along the {111} slip plane traces, bounding long microbands subdivided into slightly elongated subgrains by short lower-angle transverse subboundaries. Relatively rare cube-orientated grains displayed pronounced subdivision into coarse deformation bands containing large, low-misorientated subgrains. The misorientation vectors across subboundaries largely showed a tendency to cluster around the sample transverse direction. Apart from the rotated Goss texture component, the stored energy levels for the remaining components were principally consistent with the corresponding Taylor factor values.

A Response to Critique of the Refreeze Step in Lewin’s Model of Organizational Change from the Viewpoint of Organizational Behavior

Problem Statement
This paper responds to criticism of Kurt Lewin’s three step model of organizational change in increasingly turbulent environments. It explores whether the refreeze step of Kurt Lewin’s notable three step model is still applicable to organizational change processes in the age of globalisation and digitalisation.

Method
Literature review and critical analysis of applied examples are used to provide an overview of Kurt Lewin’s three-step change model. Authors’ observations and reflections are integrated in the discussion. The changing contemporary environment and the implications for the refreeze step of Lewin’s model are accordingly discussed.

Conclusions
The paper concludes that a balance of stability and movement; of discrete and emergent change; is the reality for today’s organizations, and forms the touchstone for Lewin’s formulation of change theories. Alignment is observed between notions of desired equilibrium in Lewin’s model and the contemporary underpinnings of sustainability. Technology and the modern pace of organizational change are also factors to consider. There has hence been an adaptation of his theoretical heritage that is current and sufficiently robust to withstand the criticisms of the refreeze stage.

The effects of escitalopram on myocardial apoptosis and the expression of Bax and Bcl-2 during myocardial ischemia/reperfusion in a model of rats with depression

BackgroundMajor depressive disorder (MDD) is an independent risk factor for coronary heart disease (CHD), and influences the occurrence and prognosis of cardiovascular events. Although there is evidence that antidepressants may be cardioprotective after acute myocardial infarction (AMI) comorbid with MDD, the operative pathophysiological mechanisms remain unclear. Our aim was therefore to explore the molecular mechanisms of escitalopram on myocardial apoptosis and the expression of Bax and Bcl-2 in a rat model of depression during myocardial ischemia/reperfusion (I/R).MethodsRats were divided randomly into 3 groups (n = 8): D group (depression), DI/R group (depression with myocardial I/R) and escitalopram + DI/R group. The rats in all three groups underwent the same chronic mild stress and separation for 21 days, at the same time, in the escitalopram + DI/R group, rats were administered escitalopram by gavage (10 mg/kg/day). Ligation of the rat¿s left anterior descending branch was done in the myocardial I/R model. Following which behavioral tests were done. The size of the myocardial infarction was detected using 1.5% TTC dye. The Tunel method was used to detect apoptotic myocardial cells, and both the Rt-PCR method and immunohistochemical techniques were used to detect the expression of Bcl¿2 and Bax.ResultsCompared with the D and DI/R groups, rats in Escitalopram + DI/R group showed significantly increased movements and sucrose consumption (P < .01). Compared with the DI/R group, the myocardial infarct size in the escitalopram + DI/R group was significantly decreased (P < .01). Compared with the D group, there were significantly increased apoptotic myocardial cells in the DI/R and escitalopram + DI/R groups (P < .01); however compared with the DI/R group, apoptotic myocardial cell numbers in the escitalopram + DI/R group were significantly decreased (P < .01). Compared with the DI/R group, there was a down-regulated Bax:Bcl-2 ratio in the escitalopram + DI/R group (P < .01).ConclusionsThese results suggest that in patients with AMI comorbid with MDD, there is an increase in pro-apoptotic pathways that is reversed by escitalopram. This suggests that clinically escitalopram may have a direct cardioprotective after acute myocardial infarction.

Evolution of strain-induced precipitates in a model austenitic Fe-30Ni-Nb steel and their effect on the flow behaviour

The present work investigated the evolution of strain-induced NbC precipitates in a model austenitic Fe-30Ni-Nb steel deformed at 925 °C to a strain of 0.2 during post-deformation holding between 3 and 1000 s and their effect on the reloading flow stress. The precipitate particles preferentially nucleated on the nodes of the periodic dislocation networks constituting microband walls. Holding for 10 s resulted in the formation of fine, largely coherent NbC particles with a mean diameter of ∼5 nm, which displayed a cube-on-cube orientation relationship with austenite and caused the maximum increase in the reloading steady-state flow stress. A further increase in the holding time from 30 to 1000 s led to the formation of semi-coherent, gradually coarser and more widely spaced particles with a mean diameter of 8 nm and above, which led to a gradual decrease in the reloading steady-state flow stress. The holding time increase resulted in progressive disintegration of the dislocation substructure and dislocation annihilation through static recovery processes, which was also reflected by the measured softening fractions. The precipitate particle shape changed during post-deformation annealing from elliptical to faceted octahedral and subsequently to tetra-kai-decahedral. © 2014 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.

Characterizing the molecular phenotype of an Atp7a(T985I) conditional knock in mouse model for X-linked distal hereditary motor neuropathy (dHMNX)

ATP7A is a P-type ATPase essential for cellular copper (Cu) transport and homeostasis. Loss-of-function ATP7A mutations causing systemic Cu deficiency are associated with severe Menkes disease or its milder allelic variant, occipital horn syndrome. We previously identified two rare ATP7A missense mutations (P1386S and T994I) leading to a non-fatal form of motor neuron disorder, X-linked distal hereditary motor neuropathy (dHMNX), without overt signs of systemic Cu deficiency. Recent investigations using a tissue specific Atp7a knock out model have demonstrated that Cu plays an essential role in motor neuron maintenance and function, however the underlying pathogenic mechanisms of ATP7A mutations causing axonal degeneration remain unknown. We have generated an Atp7a conditional knock in mouse model of dHMNX expressing Atp7a(T985I), the orthologue of the human ATP7A(T994I) identified in dHMNX patients. Although a degenerative motor phenotype is not observed, the knock in Atp7a(T985I/Y) mice show altered Cu levels within the peripheral and central nervous systems, an increased diameter of the muscle fibres and altered myogenin and myostatin gene expression. Atp7a(T985I/Y) mice have reduced Atp7a protein levels and recapitulate the defective trafficking and altered post-translational regulatory mechanisms observed in the human ATP7A(T994I) patient fibroblasts. Our model provides a unique opportunity to characterise the molecular phenotype of dHMNX and the time course of cellular events leading to the process of axonal degeneration in this disease.